scholarly journals Zinc supplementation prevents depression and deficits in spatial learning and memory associated with traumatic brain injury in the rat

2011 ◽  
Vol 25 (S1) ◽  
Author(s):  
Elise C. Cope ◽  
Jacob W. VanLandingham ◽  
Angus G. Scrimgeour ◽  
Michelle L. Condlin ◽  
Shannon D. Gower‐Winter ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Learning And Memory ◽  
Spatial Learning ◽  
Zinc Supplementation ◽  
Spatial Learning And Memory

scholarly journals Human Cerebral Organoid Implantation Alleviated the Neurological Deficits of Traumatic Brain Injury in Mice

2021 ◽  
Vol 2021 ◽  
pp. 1-16
Author(s):  
Zhongyuan Bao ◽  
Kaiheng Fang ◽  
Zong Miao ◽  
Chong Li ◽  
Chaojuan Yang ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Learning And Memory ◽  
Spatial Learning ◽  
Cortical Neurons ◽  
Embryonic Stem ◽  
High Rate ◽  
Neurological Deficits ◽  
Spatial Learning And Memory ◽  
Electromyographic Activity

Traumatic brain injury (TBI) causes a high rate of mortality and disability, and its treatment is still limited. Loss of neurons in damaged area is hardly rescued by relative molecular therapies. Based on its disease characteristics, we transplanted human embryonic stem cell- (hESC-) derived cerebral organoids in the brain lesions of controlled cortical impact- (CCI-) modeled severe combined immunodeficient (SCID) mice. Grafted organoids survived and differentiated in CCI-induced lesion pools in mouse cortical tissue. Implanted cerebral organoids differentiated into various types of neuronal cells, extended long projections, and showed spontaneous action, as indicated by electromyographic activity in the grafts. Induced vascularization and reduced glial scar were also found after organoid implantation, suggesting grafting could improve local situation and promote neural repair. More importantly, the CCI mice’s spatial learning and memory improved after organoid grafting. These findings suggest that cerebral organoid implanted in lesion sites differentiates into cortical neurons, forms long projections, and reverses deficits in spatial learning and memory, a potential therapeutic avenue for TBI.

scholarly journals Germacrone alleviates neurological deficits following traumatic brain injury by modulating neuroinflammation and oxidative stress

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Sujing Zhuang ◽  
Baogui Liu ◽  
Shifeng Guo ◽  
Yanzhong Xue ◽  
Lin Wu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Learning And Memory ◽  
Spatial Learning ◽  
Neuronal Apoptosis ◽  
Spatial Learning And Memory ◽  
Dependent Manner ◽  
Dose Dependent ◽  
And Oxidative Stress

Abstract Background Germacrone (GM) is a terpenoid compound which is reported to have anti-inflammatory and anti-oxidative effects. However, its role in treating traumatic brain injury (TBI) remains largely unknown. Methods Male C57BL/6 mice were divided into the following groups: control group, TBI group [controlled cortical impact (CCI) model], CCI + 5 mg/kg GM group, CCI + 10 mg/kg GM group and CCI + 20 mg/kg GM group. GM was administered via intraperitoneal injection. The neurological functions (including motor coordination, spatial learning and memory abilities) and brain edema were measured. Nissl staining was used to detect the neuronal apoptosis. Colorimetric assays and enzyme linked immunosorbent assay (ELISA) kits were used to determine the expression levels of oxidative stress markers including myeloperoxidase (MPO), malondialdehyde (MDA) and superoxide dismutase (SOD), as well as the expressions of inflammatory markers, including tumor necrosis factor α (TNF-α), interleukin-1β (IL-1β) and interleukin-6 (IL-6). Additionally, protein levels of Nrf2 and p-p65 were detected by Western blot assay. Results GM significantly ameliorated motor dysfunction, spatial learning and memory deficits of the mice induced by TBI and it also reduced neuronal apoptosis and microglial activation in a dose-dependent manner. Besides, GM treatment reduced neuroinflammation and oxidative stress compared to those in the CCI group in a dose-dependent manner. Furthermore, GM up-regulated the expression of antioxidant protein Nrf2 and inhibited the expression of inflammatory response protein p-p65. Conclusions GM is a promising drug to improve the functional recovery after TBI via repressing neuroinflammation and oxidative stress.

scholarly journals Long-Term Cognitive Deficits After Traumatic Brain Injury Associated With Microglia Activation

2021 ◽  
Author(s):  
Esber Saba ◽  
Mona Karout ◽  
Leila Nasralla ◽  
Firas Kobeissy ◽  
Hala Darwish ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Learning And Memory ◽  
Cognitive Deficits ◽  
Head Injuries ◽  
Spatial Learning And Memory ◽  
Post Injury ◽  
Color Flow ◽  
Injured Brain ◽  
The Central Nervous System

Abstract Traumatic Brain Injury (TBI) is the most prevalent of all head injuries, and based on the severity of the injury, it may result in chronic neurologic and cognitive deficits. Microglia play an essential role in homeostasis and diseases of the central nervous system. We hypothesize that microglia may play a beneficial or detrimental role in TBI depending on their state of activation and duration.In the present study, we evaluated whether TBI results in a spatiotemporal change in microglia phenotype and whether it affects sensory-motor or learning and memory functions in male C57BL/6 mice. We used a panel of neurological and behavioral tests and a multi-color flow cytometry-based data analysis followed by unsupervised clustering to evaluate isolated microglia from injured brain tissue. We characterized several microglial phenotypes and their association with cognitive deficits. TBI results in a spatiotemporal increase in highly activated microglia that correlated negatively with spatial learning and memory at 35 days post-injury. These observations could define therapeutic windows and accelerate translational research to improve patient outcomes.

Sign in / Sign up

Export Citation Format

Share Document